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Analysis of a uteroglobin gene polymorphism in childhood Henoch–Schonlein purpura
by
Choi, Moonsuk
, Eisenstein, Eli M.
in
Arthritis
/ Child
/ Child, Preschool
/ Female
/ Gene Frequency
/ Genetic Predisposition to Disease
/ Genotype & phenotype
/ Hematuria
/ Humans
/ Infant
/ Kidney diseases
/ Male
/ Patients
/ Pediatrics
/ Polymorphism
/ Polymorphism, Genetic
/ Purpura
/ Purpura, Schoenlein-Henoch - genetics
/ Uteroglobin - genetics
2006
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Analysis of a uteroglobin gene polymorphism in childhood Henoch–Schonlein purpura
by
Choi, Moonsuk
, Eisenstein, Eli M.
in
Arthritis
/ Child
/ Child, Preschool
/ Female
/ Gene Frequency
/ Genetic Predisposition to Disease
/ Genotype & phenotype
/ Hematuria
/ Humans
/ Infant
/ Kidney diseases
/ Male
/ Patients
/ Pediatrics
/ Polymorphism
/ Polymorphism, Genetic
/ Purpura
/ Purpura, Schoenlein-Henoch - genetics
/ Uteroglobin - genetics
2006
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Analysis of a uteroglobin gene polymorphism in childhood Henoch–Schonlein purpura
by
Choi, Moonsuk
, Eisenstein, Eli M.
in
Arthritis
/ Child
/ Child, Preschool
/ Female
/ Gene Frequency
/ Genetic Predisposition to Disease
/ Genotype & phenotype
/ Hematuria
/ Humans
/ Infant
/ Kidney diseases
/ Male
/ Patients
/ Pediatrics
/ Polymorphism
/ Polymorphism, Genetic
/ Purpura
/ Purpura, Schoenlein-Henoch - genetics
/ Uteroglobin - genetics
2006
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Analysis of a uteroglobin gene polymorphism in childhood Henoch–Schonlein purpura
Journal Article
Analysis of a uteroglobin gene polymorphism in childhood Henoch–Schonlein purpura
2006
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Overview
Uteroglobin (UG) is a pleiotropic protein with anti-inflammatory properties. Mice rendered genetically incapable of expressing UG develop a form of renal disease that closely resembles human IgA nephropathy (IgAN). Furthermore, a single nucleotide polymorphism in the UG gene (A38G) has been associated with rapid progression of human IgAN. We examined whether the A38G polymorphism is associated with childhood Henoch-Schonlein purpura (HSP), a form of vasculitis associated with IgAN-like renal disease. We examined the prevalence of the A38G polymorphism in 34 children with HSP and in 38 ethnically matched controls. Only one patient had clinically evident renal involvement. As compared with controls, the prevalence of the 38G allele was slightly increased in children with HSP, but this increase was not statistically significant. Our results do not support a role for UG in susceptibility to childhood HSP in the population studied. Larger studies involving more patients with renal disease will be necessary to define whether UG is associated with increased risk for HSP nephritis.
Publisher
Springer Nature B.V
Subject
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